Sunday, March 6, 2011
As an experiment, I submitted my last blog to Taki’s Magazine. You can judge the result for yourself. Their use of a scarred Rwandan above the title, “The Thug Gene?” was an interesting choice, I guess. Renaming MAOA seems unnecessary to me, since it was already widely known as “the warrior gene,” and ABC News also renamed it “the gangsta gene.” Likewise, yours truly has a new moniker:
“Walter Ward is a retired biology teacher. He lives in Florida and has eight grand children [sic].”
For the record, none of that is the case. I would prefer not to reveal my identity at this time, but lying, especially when the identity so easily fits a dismissible stereotype, seems counterproductive.
A couple edits to the essay changed my meaning. The article now claims that less than 1% of the whites in Rosenberg et al had the 2-repeat allele of MAOA. Just to be clear and precise, that study claimed that 2% of whites had alleles other than 3-repeats or 4-repeats, but it did not detail the exact percentage with 2-repeats for whites or African Americans. Also, the article now claims that there were four men included in the 14 total “afflicted” with Brunner syndrome, who also “escaped having the syndrome.” What I wrote was that these four had the mutation but not the syndrome. As I re-examine the only paper to mention these men, I see that there is some ambiguity as to whether they were included in the total 14, but they did not have a diagnosis by the standard of the Diagnostic and Statistical Manual of Mental Disorders (DSM, the Bible of psychiatry).
Overall, I was impressed that the editors at least wanted to check my sources. I wish they had been so careful when Michelle Malkin attacked the First Lady’s attempts to promote breastfeeding with the flippant and apocryphal claim that “the health advantages of bosom over bottle are short-lived.” Malkin gets an official pass from me though because she is soooooo gorgeous. What can I say? I recently became a very dirty, old man.
Friday, March 4, 2011
Journalism, like any art form, has genres. There is a popular celebrity-fall-from-grace genre. There is the up-and-coming cable-television-political-commentator-zings-opposing-network-political-commentator genre. One particularly controversial genre is the scientists-discover-the-fill-in-the-blank-gene genre, with usually superficial and forgettable entries. However, I would submit that there is at least one gene for something, and it concerns one of society’s ugliest controversies, the stereotype of the black male thug.
I am referring to a gene called monoamine oxidase A, or MAOA. This gene produces an enzyme that breaks down the neurotransmitters that activate many of the brain’s circuits. Back in the 1990’s, scientists discovered a mutation of MAOA that completely turns it off. The result is called Brunner syndrome, which only 14 related men have been known to have (plus animal models). What makes this extremely rare mutation so important is that it proves that MAOA really is a violent delinquency gene. A man with Brunner syndrome is what expert psychiatrists refer to as “a bad guy.” Five of these men were arsonists. Some of the men were rapists or attempted killers. Inexplicably, four men with the mutation somehow escaped having the syndrome, but for men with the mutation, those are not good odds. Nevertheless, out of the approximately three-and-a-half-billion men in the world, 14 really are not that many. Trust me, your neighbor—the one with the motorcycle—is probably not one of them. In conclusion, out of sight, out of mind.
Then came the 2000’s. The MAOA gene has a portion with repeated segments of DNA. This section of the gene is called a promoter because having more repeats increases the amount of enzyme that the gene produces (with a rare, debatable exception). After a 2002 study found that having three repeats together with having suffered child abuse is somewhat associated with violent tendencies, a flood of follow-up research ensued, and MAOA was relabeled “the warrior gene.” This version of the gene and one with four repeats are the most common versions, or alleles. These studies always had a few people with neither the 3-repeat nor the 4-repeat allele. A small number only had 2-repeats. The scientists decided that having 2-repeats in the promoter is sort of like having 3-repeats, so they invented the term “MAOA-L.” (“L” stands for low. Pretty clever, huh?) However, a pair of studies in 2008 found that the 2-repeat allele is associated with twice the rate of violence without child abuse coming into the equation. This allele is less powerful than Brunner syndrome but far more common.
Two small studies gave hints that the especially dangerous 2-repeat allele might be more common among African Americans. One study wrote that 6% of their non-white (but probably mostly African-American) male subjects had this allele. The other had 5 of 37 (14%) African-American men possessing “rare MAOA alleles.” Those percentages are remarkable given that studies of white men have suggested that 1% or fewer have this gene.
If a single gene could offer some explanation as to why African-Americans commit roughly five times as many violent crimes per capita as whites, then wouldn’t studying it potentially save countless lives and deserve a Nobel Prize? After all, even a case of Brunner syndrome was effectively treated for a period with an antipsychotic. Well, at long last, Reti et al determined that 0.5% of white MAOA genes and 4.7% of African-American MAOA genes are this 2-repeat allele, almost a ten-fold difference.
Hopefully, for the sake of improved diagnosis and treatment, a small number of genes like MAOA greatly influence societal problems like violent delinquency. However, some studies suggest that the genetics of behavior is spread diffusely among many genes. Science must also examine the complex web of gene-environment, gene-hormone, and gene-gene interactions. As the price of decoding genomes declines, it will become easier to develop software that analyzes standardized behavioral and developmental metrics and multiple gene elements for sundry associations.
Consider the study Beaver et al from about one year ago. This was a study of African-American men and five violence genes that reached the shocking conclusion that a crude genetic index of these genes predicted adult violent delinquency better than a detailed measure of the quality of the men’s childhood relationship with their respective mothers. This finding is all the more impressive given how unimpressive the gene index was. Each allele was assigned a point. A 2-repeat allele of MAOA was worth the same as a 3-repeat allele of MAOA and the same as an allele of another gene that had limited evidence of impacting violent behavior. Also, MAOA is on the X chromosome, meaning that these men only had one copy, unlike the other genes, which come in pairs. So, apparently having a 2-repeat allele was actually worth only half as much as each pair of the other genes. This study could be improved upon by follow up research that weights the genes differently using a computer program that could compare multitudinous reiterations to determine the optimum weights.
After following research on the genetics of violence for years now, I am convinced that the various alleles of MAOA affect violent behavior in white men and black men. Thus, the differing frequencies of these alleles might contribute to the differing rates of violent crime. I am sensitive to the fact that this line of research could reinforce unfair judgments that all black men are dangerous, but the 2-repeat allele of MAOA illustrates that a gene might contribute to a racial disparity in violent behavior even though most black men do not have said allele. If it is an important violence gene, then maybe targeted treatments can be created that will be more likely to help African-American men and bring American society closer to equality. In other words, medical and scientific ethics should be informed by both the improved standards of moral responsibility since the end of the eugenics era and a mature, realistic appreciation of the coming genetics era.